↵∗Division of Cardiovascular Sciences, St. George’s University of London, Cranmer Terrace, London SW17 0RE, United Kingdom

We are grateful to Dr. La Gerche and colleagues for their interest in our paper (1). They cite their recent study that presents an intriguing anatomic explanation for T-wave inversion (TWI) in athletes, namely, that training-induced lateral cardiac displacement presents a greater proportion of the right ventricle to the anterior precordial electrocardiography leads, creating negative repolarization potentials (2). Although this hypothesis has merit from the perspective of vector cardiography, it seems unlikely that cardiac rotation alone should account for the spectrum of repolarization changes in athletic individuals. The authors illustrate their hypothesis with an example of marked lateral cardiac displacement in an athlete, yet the corresponding electrocardiogram reveals only very subtle T-wave changes. This is in stark contrast with the deep TWI, often in excess of −0.5 mV, that is frequently present in healthy athletes. Additionally, one should not discount completely the potential role of the left ventricle, which may constitute 5 times the mass of the right ventricle in some athletes, in the genesis of T-wave changes. The similarity between TWI in endurance athletes and patients presenting with acute anterior myocardial infarction is remarkable; we previously demonstrated left ventricular wall thickness to be an independent predictor of TWI in athletes (3). Perhaps the most persuasive argument against a simple mechanical explanation for TWI can be found in the 14% of African and Afro-Caribbean athletes who reveal deep anterior TWI (3,4). It seems unlikely that lateral cardiac displacement should account for this striking anomaly in so many cases. We previously documented right ventricular (RV) dimensions to be similar in black and Caucasian athletes and found no association between RV size and TWI (4). The aforementioned study from La Gerche’s group supports the latter finding; therefore, it is difficult to understand the proposed mechanism behind training-induced lateral cardiac displacement if not driven by ventricular enlargement. The associations between athletic activity, cardiac rotation, and anterior TWI reported by La Gerche et al. require corroboration in longitudinal studies of athletes in various states of detraining before any causal relationships can be inferred.

We agree entirely that anterior TWI in the context of sinister cardiovascular symptoms should raise suspicion of primary or indeed exercise-induced arrhythmogenic RV cardiomyopathy. We also agree that the high prevalence of anterior TWI in asymptomatic athletes suggests physiological remodeling in most cases. However, these repolarization changes probably represent the complex interplay between structural, functional, and electrical remodeling forces that we have yet to fully comprehend.

Footnotes

Please note: Drs. Zaidi, Sheikh, Gati, and Papadakis were funded by research grants from the charitable organization Cardiac Risk in the Young (CRY). Dr. Sharma has been a coapplicant on previous grants from CRY to study athletes and nonathletes. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

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